The frequency of the diagnosis of takotsubo cardiomyopathy has increased rapidly over the past few years, possibly due to increasing awareness among cardiologists. At initial presentation the diagnosis remains a challenge because of the close similarity between the presentation of takotsubo cardiomyopathy, and that of ST elevation myocardial infarction (STEMI). Recognition of salient aspects of the medical history at presentation are important in order to organise further appropriate investigations such as echocardiography and left ventriculography at the time of coronary angiogram. Takotsubo cardiomyopathy can be easily missed without ventriculography early after presentation because of the transient nature of left ventricular dysfunction, and in many centres left ventriculogram is not done as standard in the setting of STEMI. The authors advocate left ventriculography in all cases of ST elevation who have unobstructed coronaries. The correct diagnosis of takotsubo cardiomyopathy is very important for future advice and management of the patient. The prognosis of this condition is generally excellent with almost all patients returning to normal within a few weeks. This article examines the takotsubo cardiomyopathy literature and discusses the pathophysiology, clinical features, management, and prognosis of this condition in the context of an illustrated case.

Previous clinical studies have shown heterogeneity in individual patient responses to antiplatelet therapy and high residual platelet reactivity is associated with increased risk of adverse clinical events. Monitoring response to antiplatelet therapy and tailoring treatment accordingly is currently not recommended in routine clinical practice largely due to the lack of a standardized definition of antiplatelet therapy hyporesponse and the need for a widely accepted point-of-care platelet function test that can be reliably utilized in frontline clinical practice. Recent data have shown that titrating the dose of clopidogrel in patients undergoing percutaneous coronary intervention significantly reduces the incidence of major adverse cardiovascular events and large-scale clinical trials are currently underway to investigate whether individually tailored treatment based on results of platelet function testing leads to improved clinical outcome. Furthermore, genetic testing has demonstrated a link between CYP2C19 genetic polymorphisms, altered clopidogrel metabolite concentrations and adverse clinical events. Clinical studies are currently underway to investigate the potential clinical benefit associated with genotype-guided tailoring of antiplatelet therapy. With the advent of newer, more potent antiplatelet agents and their associated increased bleeding risks, it will become imperative in the future to select the most appropriate, safe and effective drug.

Dual antiplatelet therapy with aspirin and clopidogrel is routinely indicated in patients with acute coronary syndromes and following percutaneous coronary intervention to reduce the risk of cardiovascular mortality and ischaemic events. Although clinical guidelines recommend aspirin lifelong and clopidogrel for between one and 12 months, depending upon the indication, the optimal duration of clopidogrel therapy actually remains contentious. Premature cessation of clopidogrel in patients receiving drug-eluting stents is a clear risk factor for stent thrombosis, but recent clinical studies have also demonstrated a link between "appropriate" cessation of clopidogrel and clustering of adverse clinical events. It has been suggested that this may be due to a "rebound" prothrombotic and/ or proinflammatory response associated with clopidogrel withdrawal. This review will examine the definition and concept of a "rebound" phenomenon associated with clopidogrel cessation as well as the likely mechanisms behind this effect. Within the context of clinical event clustering after clopidogrel cessation, we will also discuss (i) the clinical importance of clopidogrel and the increasing uncertainty surrounding optimal duration of therapy, (ii) the antiplatelet and anti-inflammatory properties of clopidogrel and, in particular, its influence on arachidonic acid pathways traditionally thought to be mediated predominantly by aspirin and (iii) the role of newer, more potent antiplatelet agents and potential changes to antiplatelet therapy prescribing guidelines in the future.

There is a high prevalence of hyporesponsiveness to APT in patients with ST. Improved APT efficacy can be achieved by tailored therapy. Short TEG is a plausible platelet function test that can be used to deliver point of care personalised APT.